Here's another old post of mine, that may be relevant to this thread as well, regarding stress:
There are certain signs that stress can play an important role with tinnitus, and more studies in this area may begin to show some solid conclusive proof. There is some evidence however - scientific and anecdotal - that shows stress is a very important contributor.
A common feature of burnout syndrome, for example, is tinnitus. Why is this? You could find a relationship between excessive cortisol levels in the bloodstream - over an extended period of time - and problems with tinnitus arising or getting worse. There is certainly a lot of evidence to support this from the frequent reports of tinnitus arising after intense periods of emotional stress. Excessive cortisol is not good for us and can cause all kinds of problems if left unchecked. Another issue is that many people are simply unaware that their cortisol levels are high, as they adapt or get used to it. Stress in this instance is a hidden danger.
Here is a link explaining more on the subject; I will copy and paste the content below:
http://www.deutsche-tinnitus-stiftung-charite.de/en/projects/tinnitus_and_stress/
"
Many people who suffer from tinnitus believe that stress is the cause. And first studies indicate that there is indeed a connection. What is lacking is scientific proof.
The project "Influence of emotional stress on auditory functions" (for short: "Tinnitus and Stress") is contributing to remedying this lack. It draws on research done by the molecular biology research laboratory of the ENT Clinic and the Tinnitus Center Charité.
It is established that chronic stress can in general induce and exacerbate changes to the auditory system. They include above all thehypersensitization of auditory perception (hyperacusis), tinnitus, and Menière's disease, a disorder of the inner ear that leads to attacks of rotatory vertigo, one-sided hearing loss, and ringing in the ears.
But how does stress arise? As a rule it develops when people cannot cope with the growing and/or unexpected demands of their environment. They live under constant emotional pressure. The most frequent reaction is to deny any physical risk in an effort to enhance one's own achievement potential and staying power.
The physical effects of stress include increased production of the stress hormone cortisol. This raises the blood sugar level (gluconeogenesis) and intensifies the breakdown of stored fat (lipolysis), as well as protein breakdown (proteolysis), making more energy available. Higher blood pressure, a high pulse rate, and constipation are the result. But the immune system also suffers. Many patients complain of sleeplessness and a lack of appetite, psychomotor disturbances, and growing feelings of anxiety.
According to Professor Birgit Mazurek, "All these stress-induced mental changes can also influence auditory phenomena, leading, for example to the development of tinnitus or the exacerbation of an existing tinnitus. In the ear, cortisol causes a massive release of glutamate into the neurons. This ultimately leads to a greater accumulation of calcium, which damages auditory sensory cells and nerve cells in the ear."
With the "Stress and Tinnitus" project, the Foundation seeks to promote research in this field to develop better individual therapeutic approaches for patients with tinnitus and hyperacusis.
The HEINZ AND HEIDE DÜRR FOUNDATION is contributing € 150,000 over a period of three years to fund the research project."
Here is another study that finds evidence of stress having a direct effect on tinnitus. Again, I will quote some excerpts below, but I highly recommend reading the whole study:
http://www.biomedcentral.com/1472-6815/12/4
"We report three novel findings that establish differences between tinnitus participants and controls in terms of cortisol hypersuppression, longer-lasting effects of the DEX test on basal cortisol levels, and hearing discomfort threshold. The first novel finding is that tinnitus participants had more strongly suppressed cortisol levels than controls after pharmacological challenge, despite similar basal cortisol levels. This is consistent with the normal diurnal and blunted response to psychosocial stress in tinnitus participants described in a previous study [
23], and supports the hypothesis that tinnitus participants have greater sensitivity to HPA axis negative feedback. Hypersuppression in the presence of normal or near-normal basal cortisol levels has also been found in other clinical populations, such as patients with chronic fatigue syndrome [
45–
47] and burnout [
48]. All these findings are consistent with the notion that basal cortisol and post-DEX cortisol suppression are mediated by two separate receptor feedback systems. More importantly, the suppression effect was independent of hearing loss. This is a key finding, because these factors are difficult to disentangle in tinnitus studies [
19,
23], and it argues for a true effect of tinnitus in addition to, but unrelated to, hearing loss. Our findings therefore directly link tinnitus to a stress-related disorder, and not just to a hearing-related disorder, as some recent population studies suggest [
12,
49].
The second important finding is that tinnitus participants showed a long-lasting carryover effect of cortisol manipulation. They had lower basal cortisol the day after the post-DEX day assessment compared to the two other basal cortisol assessment days, indicating not only cortisol hypersuppression, but also a longer-lasting effect of DEX administration. Although it cannot be excluded that these findings could be related to slower DEX clearance in these patients, this possibility is unlikely, because there is no rationale for altered liver function in this particular group, which moreover did not differ from controls in terms of age, BMI, or physical or mental health. Furthermore, the carryover effect was observed in the tinnitus participants approximately 36 hours after DEX administration, whereas cortisol and DEX levels should return to baseline 24 hours after oral administration of 0.5 mg DEX [
50]. A likely interpretation is that the carryover effect might have been due to HPA axis homeostatic vulnerability, and that hypersuppression might have been caused by increased glucocorticoid sensitivity."
"Subjective tinnitus ("tinnitus") is the perception of sound in the ears or head in the absence of an external sound and difficult to treat. Individuals with tinnitus can experience severe emotional distress, depression, anxiety, and insomnia [
1–
5]. A recent study in 14,278 adults reported anoverall prevalence of 25.3% for any experience of tinnitus in the previous year and 7.9% for frequent or constant (at least once a day) tinnitus [
6]. Prevalence increases with age, peaking at 31.4% and 14.3% from age 60 to 69 years for these two tinnitus frequencies, respectively [
6]. The increasing prevalence with age is not surprising, because hearing loss is known to be an associated risk factor for tinnitus [
7]. With increasing life expectancy, and because hearing loss and noise exposure are increasingly affecting military personnel [
8,
9] and youth [
10], tinnitus has become a significant public health issue.
Hearing loss predicts tinnitus presence, but not severity [
11,
12]. Conversely, individuals with hearing loss do not necessarily experience tinnitus. There is therefore a need to determine other factors for this debilitating hearing disorder and its consequences for health in order to better prevent and treat it. One likely candidate is stress. Because stress has long been identified as a trigger or co-morbidity of tinnitus, based mainly on anecdotal and retrospective reports, this idea has been taken for granted in classical teachings on tinnitus [
13]. In addition, recent large population studies have established that emotional exhaustion and long-term stress are predictors of hearing disorders, including tinnitus [
14,
15]. Functional and electroencephalographic brain imaging studies have also shown aberrant links between limbic (involved in emotions) and auditory system structures [
16–
18]. Structural brain differences (i.e., grey matter decrease) in tinnitus involving parts of the limbic system have also been reported. More specifically, less grey matter in the nucleus accumbens [
18,
19] and the left hippocampus [
20] suggests a depletion that could be related to long-term exposure to stress, among other factors."
"Our findings suggest heightened glucocorticoid sensitivity in tinnitus in terms of an abnormally strong GR-mediated HPA-axis feedback (despite a normal MR-mediated tone) and lower tolerance for sound loudness with suppressed cortisol levels. Long-term stress exposure and its deleterious effects therefore constitute an important predisposing factor for, or a significant pathological consequence of, this debilitating hearing disorder."
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